Pub Date : 2014-12-31DOI: 10.4161/23328940.2014.980138
A. Flouris
Developing a unifying theory for the functional architecture of endothermic thermoregulation has been proven to be a challenging endeavor. Three papers published in this issue of Temperature take a closer look at this problem and add interesting views to our knowledge about the way that endothermic thermoregulation works.
{"title":"A unifying theory for the functional architecture of endothermic thermoregulation","authors":"A. Flouris","doi":"10.4161/23328940.2014.980138","DOIUrl":"https://doi.org/10.4161/23328940.2014.980138","url":null,"abstract":"Developing a unifying theory for the functional architecture of endothermic thermoregulation has been proven to be a challenging endeavor. Three papers published in this issue of Temperature take a closer look at this problem and add interesting views to our knowledge about the way that endothermic thermoregulation works.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"10 1","pages":"162 - 163"},"PeriodicalIF":0.0,"publicationDate":"2014-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90120046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-12-31DOI: 10.4161/23328940.2014.980137
E. Kiyatkin, Suelynn Ren
In this issue, Parrot and Young present the results of temperature measurements in young individuals “partying” with 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy). This editorial commentary briefly summarizes the main findings of their study, provides background gained from previous animal experiments, and reviews the implications for the development of future pharmacotherapies and harm reduction strategies.
{"title":"Clubbing with ecstasy","authors":"E. Kiyatkin, Suelynn Ren","doi":"10.4161/23328940.2014.980137","DOIUrl":"https://doi.org/10.4161/23328940.2014.980137","url":null,"abstract":"In this issue, Parrot and Young present the results of temperature measurements in young individuals “partying” with 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy). This editorial commentary briefly summarizes the main findings of their study, provides background gained from previous animal experiments, and reviews the implications for the development of future pharmacotherapies and harm reduction strategies.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"29 1","pages":"160 - 161"},"PeriodicalIF":0.0,"publicationDate":"2014-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83447134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-12-31DOI: 10.4161/23328940.2014.982048
D. Ramsay, K. Kaiyala, S. Woods
Homeostasis stabilizes critical biological variables within appropriate limits via corrective regulatory effector responses that adequately counter disturbing effects. Identifying individual effects and responses, and distinguishing their individual influences on a regulated state, is challenging. Studying effector responses can reveal regulatory phenomena that depart from homeostasis into the realm of allostasis.
{"title":"Correctly identifying responses is critical for understanding homeostatic and allostatic regulation","authors":"D. Ramsay, K. Kaiyala, S. Woods","doi":"10.4161/23328940.2014.982048","DOIUrl":"https://doi.org/10.4161/23328940.2014.982048","url":null,"abstract":"Homeostasis stabilizes critical biological variables within appropriate limits via corrective regulatory effector responses that adequately counter disturbing effects. Identifying individual effects and responses, and distinguishing their individual influences on a regulated state, is challenging. Studying effector responses can reveal regulatory phenomena that depart from homeostasis into the realm of allostasis.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"4 1","pages":"157 - 159"},"PeriodicalIF":0.0,"publicationDate":"2014-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73701859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-12-31DOI: 10.4161/23328940.2014.982047
E. Nalivaiko, J. Rudd, R. So
Principal symptoms of motion sickness in humans include facial pallor, nausea and vomiting, and sweating. It is less known that motion sickness also affects thermoregulation, and the purpose of this review is to present and discuss existing data related to this subject. Hypothermia during seasickness was firstly noted nearly 150 years ago, but detailed studies of this phenomenon were conducted only during the last 2 decades. Motion sickness-induced hypothermia is philogenetically quite broadly expressed as besides humans, it has been reported in rats, musk shrews and mice. Evidence from human and animal experiments indicates that the physiological mechanisms responsible for the motion sickness-induced hypothermia include cutaneous vasodilation and sweating (leading to an increase of heat loss) and reduced thermogenesis. Together, these results suggest that motion sickness triggers highly coordinated physiological response aiming to reduce body temperature. Finally, we describe potential adaptive role of this response, and describe the benefits of using it as an objective measure of motion sickness-induced nausea.
{"title":"Motion sickness, nausea and thermoregulation: The “toxic” hypothesis","authors":"E. Nalivaiko, J. Rudd, R. So","doi":"10.4161/23328940.2014.982047","DOIUrl":"https://doi.org/10.4161/23328940.2014.982047","url":null,"abstract":"Principal symptoms of motion sickness in humans include facial pallor, nausea and vomiting, and sweating. It is less known that motion sickness also affects thermoregulation, and the purpose of this review is to present and discuss existing data related to this subject. Hypothermia during seasickness was firstly noted nearly 150 years ago, but detailed studies of this phenomenon were conducted only during the last 2 decades. Motion sickness-induced hypothermia is philogenetically quite broadly expressed as besides humans, it has been reported in rats, musk shrews and mice. Evidence from human and animal experiments indicates that the physiological mechanisms responsible for the motion sickness-induced hypothermia include cutaneous vasodilation and sweating (leading to an increase of heat loss) and reduced thermogenesis. Together, these results suggest that motion sickness triggers highly coordinated physiological response aiming to reduce body temperature. Finally, we describe potential adaptive role of this response, and describe the benefits of using it as an objective measure of motion sickness-induced nausea.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"27 1","pages":"164 - 171"},"PeriodicalIF":0.0,"publicationDate":"2014-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76400076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-12-31DOI: 10.4161/23328940.2014.978716
A. Ivanov
This Editorial is written to introduce Tissue Barriers, a new Taylor & Francis journal, to the readers of Temperature. It describes the role of temperature in the regulation of different tissue barriers under normal and disease conditions. It also highlights the most interesting articles published in the first volume of Tissue Barriers.
{"title":"Tissue Barriers: Introducing an exciting new journal","authors":"A. Ivanov","doi":"10.4161/23328940.2014.978716","DOIUrl":"https://doi.org/10.4161/23328940.2014.978716","url":null,"abstract":"This Editorial is written to introduce Tissue Barriers, a new Taylor & Francis journal, to the readers of Temperature. It describes the role of temperature in the regulation of different tissue barriers under normal and disease conditions. It also highlights the most interesting articles published in the first volume of Tissue Barriers.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"1 1","pages":"151 - 153"},"PeriodicalIF":0.0,"publicationDate":"2014-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84078954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-12-10DOI: 10.4161/23328940.2014.977182
A. Parrott, L. Young
Aims and rationale: to investigate body temperature and thermal self-ratings of Ecstasy/MDMA users at a Saturday night dance club. Methods: 68 dance clubbers (mean age 21.6 years, 30 females and 38 males), were assessed at a Saturday night dance club, then 2–3 d later. Three subgroups were compared: 32 current Ecstasy users who had taken Ecstasy/MDMA that evening, 10 abstinent Ecstasy/MDMA users on other psychoactive drugs, and 26 non-user controls (predominantly alcohol drinkers). In a comparatively quiet area of the dance club, each unpaid volunteer had their ear temperature recorded, and completed a questionnaire on thermal feelings and mood states. A similar questionnaire was repeated 2–3 d later by mobile telephone. Results: Ecstasy/MDMA users had a mean body temperature 1.2°C higher than non-user controls (P < 0.001), and felt significantly hotter and thirstier. The abstinent Ecstasy/MDMA polydrug user group had a mean body temperature intermediate between the other 2 groups, significantly higher than controls, and significantly lower than current Ecstasy/MDMA users. After 2–3 d of recovery, the Ecstasy/MDMA users remained significantly ‘thirstier’. Higher body temperature while clubbing was associated with greater Ecstasy/MDMA usage at the club, and younger age of first use. Higher temperature also correlated with lower elation and poor memory 2–3 d later. It also correlated positively with nicotine, and negatively with cannabis. Conclusions: Ecstasy/MDMA using dance clubbers had significantly higher body temperature than non-user controls. This heightened body temperature was associated with a number of adverse psychobiological consequences, including poor memory.
{"title":"Saturday night fever in ecstasy/MDMA dance clubbers: Heightened body temperature and associated psychobiological changes","authors":"A. Parrott, L. Young","doi":"10.4161/23328940.2014.977182","DOIUrl":"https://doi.org/10.4161/23328940.2014.977182","url":null,"abstract":"Aims and rationale: to investigate body temperature and thermal self-ratings of Ecstasy/MDMA users at a Saturday night dance club. Methods: 68 dance clubbers (mean age 21.6 years, 30 females and 38 males), were assessed at a Saturday night dance club, then 2–3 d later. Three subgroups were compared: 32 current Ecstasy users who had taken Ecstasy/MDMA that evening, 10 abstinent Ecstasy/MDMA users on other psychoactive drugs, and 26 non-user controls (predominantly alcohol drinkers). In a comparatively quiet area of the dance club, each unpaid volunteer had their ear temperature recorded, and completed a questionnaire on thermal feelings and mood states. A similar questionnaire was repeated 2–3 d later by mobile telephone. Results: Ecstasy/MDMA users had a mean body temperature 1.2°C higher than non-user controls (P < 0.001), and felt significantly hotter and thirstier. The abstinent Ecstasy/MDMA polydrug user group had a mean body temperature intermediate between the other 2 groups, significantly higher than controls, and significantly lower than current Ecstasy/MDMA users. After 2–3 d of recovery, the Ecstasy/MDMA users remained significantly ‘thirstier’. Higher body temperature while clubbing was associated with greater Ecstasy/MDMA usage at the club, and younger age of first use. Higher temperature also correlated with lower elation and poor memory 2–3 d later. It also correlated positively with nicotine, and negatively with cannabis. Conclusions: Ecstasy/MDMA using dance clubbers had significantly higher body temperature than non-user controls. This heightened body temperature was associated with a number of adverse psychobiological consequences, including poor memory.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"58 1","pages":"214 - 219"},"PeriodicalIF":0.0,"publicationDate":"2014-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74639978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-11-17eCollection Date: 2014-10-01DOI: 10.4161/23328940.2014.984553
Ina Isabella Høiland, Louis de Weerd, James B Mercer
While health risks from smoking cigarettes are well known, little is known about the health risks of using smokeless tobacco (ST). The aim of this study was to evaluate the effect that ST in the form of oral use of snus with nicotine and snus without nicotine has on peripheral skin blood circulation. 21 young habitual users of snus with nicotine participated in this study. Under controlled conditions the subjects were exposed to a 30 minute period of oral use of snus with nicotine (SN+) and snus without nicotine (SN-). The peripheral skin blood circulation was indirectly monitored on the hands by measuring skin temperature using infrared thermography. The skin blood circulation in the hands showed a statistical significant decrease in the SN+ experiments, while skin blood circulation was hardly effected in the SN- experiments. It is concluded that the use of smokeless tobacco in the form of oral use of snus containing nicotine causes a decrease in peripheral skin blood circulation while such an effect is not seen in snus without nicotine. This knowledge may be of use when treating patients that require adequate peripheral skin circulation or in the military when soldiers are exposed cold conditions.
{"title":"The effect of oral uptake of nicotine in snus on peripheral skin blood circulation evaluated by thermography.","authors":"Ina Isabella Høiland, Louis de Weerd, James B Mercer","doi":"10.4161/23328940.2014.984553","DOIUrl":"10.4161/23328940.2014.984553","url":null,"abstract":"<p><p>While health risks from smoking cigarettes are well known, little is known about the health risks of using smokeless tobacco (ST). The aim of this study was to evaluate the effect that ST in the form of oral use of snus with nicotine and snus without nicotine has on peripheral skin blood circulation. 21 young habitual users of snus with nicotine participated in this study. Under controlled conditions the subjects were exposed to a 30 minute period of oral use of snus with nicotine (SN+) and snus without nicotine (SN-). The peripheral skin blood circulation was indirectly monitored on the hands by measuring skin temperature using infrared thermography. The skin blood circulation in the hands showed a statistical significant decrease in the SN+ experiments, while skin blood circulation was hardly effected in the SN- experiments. It is concluded that the use of smokeless tobacco in the form of oral use of snus containing nicotine causes a decrease in peripheral skin blood circulation while such an effect is not seen in snus without nicotine. This knowledge may be of use when treating patients that require adequate peripheral skin circulation or in the military when soldiers are exposed cold conditions. </p>","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"1 1","pages":"220-6"},"PeriodicalIF":0.0,"publicationDate":"2014-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73519947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-11-14DOI: 10.4161/23328940.2014.982049
J. Bowyer, J. Hanig
The adverse effects of amphetamine- (AMPH) and methamphetamine- (METH) induced hyperthermia on vasculature, peripheral organs and peripheral immune system are discussed. Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. Forebrain neurotoxicity can also be indirectly influenced through the effects of AMPH- and METH- induced hyperthermia on vasculature. The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. This BBB breakdown can occur in the amygdala, thalamus, striatum, sensory and motor cortex and hippocampus. Under these conditions, repetitive seizures greatly enhance neurodegeneration in hippocampus, thalamus and amygdala. Even when the BBB is less disrupted, AMPH- or METH- induced hyperthermia effects on brain vasculature may play a role in neurotoxicity. In this case, striatal and cortical vascular function are adversely affected, and even greater ROS, immune and damage responses are seen in the meninges and cortical surface vasculature. Finally, muscle and liver damage and elevated cytokines in blood can result when amphetamines produce hyperthermia. Proteins, from damaged muscle may activate the peripheral immune system and exacerbate liver damage. Liver damage can further increase cytokine levels, immune system activation and increase ammonia levels. These effects could potentially enhance vascular damage and neurotoxicity.
{"title":"Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity","authors":"J. Bowyer, J. Hanig","doi":"10.4161/23328940.2014.982049","DOIUrl":"https://doi.org/10.4161/23328940.2014.982049","url":null,"abstract":"The adverse effects of amphetamine- (AMPH) and methamphetamine- (METH) induced hyperthermia on vasculature, peripheral organs and peripheral immune system are discussed. Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia (≥40°C) are minimally neurotoxic. Hyperthermia likely enhances AMPH and METH neurotoxicity directly through disruption of protein function, ion channels and enhanced ROS production. Forebrain neurotoxicity can also be indirectly influenced through the effects of AMPH- and METH- induced hyperthermia on vasculature. The hyperthermia and the hypertension produced by high doses amphetamines are a primary cause of transient breakdowns in the blood-brain barrier (BBB) resulting in concomitant regional neurodegeneration and neuroinflammation in laboratory animals. This BBB breakdown can occur in the amygdala, thalamus, striatum, sensory and motor cortex and hippocampus. Under these conditions, repetitive seizures greatly enhance neurodegeneration in hippocampus, thalamus and amygdala. Even when the BBB is less disrupted, AMPH- or METH- induced hyperthermia effects on brain vasculature may play a role in neurotoxicity. In this case, striatal and cortical vascular function are adversely affected, and even greater ROS, immune and damage responses are seen in the meninges and cortical surface vasculature. Finally, muscle and liver damage and elevated cytokines in blood can result when amphetamines produce hyperthermia. Proteins, from damaged muscle may activate the peripheral immune system and exacerbate liver damage. Liver damage can further increase cytokine levels, immune system activation and increase ammonia levels. These effects could potentially enhance vascular damage and neurotoxicity.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"1930 1","pages":"172 - 182"},"PeriodicalIF":0.0,"publicationDate":"2014-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91108712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-11-14DOI: 10.4161/23328940.2014.985953
Christine K. Dao, Sara M. Nowinski, E. Mills
Thermoregulation is an essential homeostatic process in which critical mechanisms of heat production and dissipation are controlled centrally in large part by the hypothalamus and peripherally by activation of the sympathetic nervous system. Drugs that disrupt the components of this highly orchestrated multi-organ process can lead to life-threatening hyperthermia. In most cases, hyperthermic agents raise body temperature by increasing the central and peripheral release of thermoregulatory neurotransmitters that ultimately lead to heat production in thermogenic effector organs skeletal muscle (SKM) and brown adipose tissue (BAT). In many cases hyperthermic drugs also decrease heat dissipation through peripheral changes in blood flow. Drug-induced heat production is driven by the stimulation of mechanisms that normally regulate the adaptive thermogenic responses including both shivering and non-shivering thermogenesis (NST) mechanisms. Modulation of the mitochondrial electrochemical proton/pH gradient by uncoupling protein 1 (UCP1) in BAT is the most well characterized mechanism of NST in response to cold, and may contribute to thermogenesis induced by sympathomimetic agents, but this is far from established. However, the UCP1 homologue, UCP3, and the ryanodine receptor (RYR1) are established mediators of toxicant-induced hyperthermia in SKM. Defining the molecular mechanisms that orchestrate drug-induced hyperthermia will be essential in developing treatment modalities for thermogenic illnesses. This review will briefly summarize mechanisms of thermoregulation and provide a survey of pharmacologic agents that can lead to hyperthermia. We will also provide an overview of the established and candidate molecular mechanisms that regulate the actual thermogenic processes in heat effector organs BAT and SKM.
体温调节是一个重要的内稳态过程，其中热量产生和耗散的关键机制在很大程度上由下丘脑集中控制，并通过交感神经系统的激活在外围控制。破坏这种高度协调的多器官过程的药物会导致危及生命的高热。在大多数情况下，高热药物通过增加中枢和外周热调节神经递质的释放来提高体温，最终导致产热效应器官骨骼肌(SKM)和棕色脂肪组织(BAT)的产热。在许多情况下，热疗药物也会通过外周血管血流的改变来减少散热。药物诱导的产热是由通常调节适应性产热反应的机制刺激驱动的，包括寒战和非寒战产热(NST)机制。BAT中解偶联蛋白1 (uncoupling protein 1, UCP1)对线粒体电化学质子/pH梯度的调节是NST应对寒冷的最明确机制，可能有助于拟交感神经药物诱导的产热，但这还远未确定。然而，UCP1同源物、UCP3和ryanodine受体(RYR1)是SKM中毒性诱导高热的已知介质。确定协调药物诱导热疗的分子机制对于开发热源性疾病的治疗方式至关重要。本文将简要概述体温调节的机制，并提供可导致热疗的药物的调查。我们还将概述调节热效应器官BAT和SKM中实际产热过程的已建立和候选分子机制。
{"title":"The heat is on: Molecular mechanisms of drug-induced hyperthermia","authors":"Christine K. Dao, Sara M. Nowinski, E. Mills","doi":"10.4161/23328940.2014.985953","DOIUrl":"https://doi.org/10.4161/23328940.2014.985953","url":null,"abstract":"Thermoregulation is an essential homeostatic process in which critical mechanisms of heat production and dissipation are controlled centrally in large part by the hypothalamus and peripherally by activation of the sympathetic nervous system. Drugs that disrupt the components of this highly orchestrated multi-organ process can lead to life-threatening hyperthermia. In most cases, hyperthermic agents raise body temperature by increasing the central and peripheral release of thermoregulatory neurotransmitters that ultimately lead to heat production in thermogenic effector organs skeletal muscle (SKM) and brown adipose tissue (BAT). In many cases hyperthermic drugs also decrease heat dissipation through peripheral changes in blood flow. Drug-induced heat production is driven by the stimulation of mechanisms that normally regulate the adaptive thermogenic responses including both shivering and non-shivering thermogenesis (NST) mechanisms. Modulation of the mitochondrial electrochemical proton/pH gradient by uncoupling protein 1 (UCP1) in BAT is the most well characterized mechanism of NST in response to cold, and may contribute to thermogenesis induced by sympathomimetic agents, but this is far from established. However, the UCP1 homologue, UCP3, and the ryanodine receptor (RYR1) are established mediators of toxicant-induced hyperthermia in SKM. Defining the molecular mechanisms that orchestrate drug-induced hyperthermia will be essential in developing treatment modalities for thermogenic illnesses. This review will briefly summarize mechanisms of thermoregulation and provide a survey of pharmacologic agents that can lead to hyperthermia. We will also provide an overview of the established and candidate molecular mechanisms that regulate the actual thermogenic processes in heat effector organs BAT and SKM.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"25 1","pages":"183 - 191"},"PeriodicalIF":0.0,"publicationDate":"2014-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83284573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-10-31DOI: 10.4161/23328940.2014.955433
M. Liechti
Hyperthermia is a severe complication associated with the recreational use of 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy). In this review, the clinical laboratory studies that tested the effects of MDMA on body temperature are summarized. The mechanisms that underlie the hyperthermic effects of MDMA in humans and treatment of severe hyperthermia are presented. The data show that MDMA produces an acute and dose-dependent rise in core body temperature in healthy subjects. The increase in body temperature is in the range of 0.2-0.8°C and does not result in hyperpyrexia (>40°C) in a controlled laboratory setting. However, moderately hyperthermic body temperatures >38.0°C occur frequently at higher doses, even in the absence of physical activity and at room temperature. MDMA primarily releases serotonin and norepinephrine. Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation. The mediating role of serotonin is unclear. The management of sympathomimetic toxicity and associated hyperthermia mainly includes sedation with benzodiazepines and intravenous fluid replacement. Severe hyperthermia should primarily be treated with additional cooling and mechanical ventilation.
{"title":"Effects of MDMA on body temperature in humans","authors":"M. Liechti","doi":"10.4161/23328940.2014.955433","DOIUrl":"https://doi.org/10.4161/23328940.2014.955433","url":null,"abstract":"Hyperthermia is a severe complication associated with the recreational use of 3,4-methylenedioxymethamphetamine (MDMA, Ecstasy). In this review, the clinical laboratory studies that tested the effects of MDMA on body temperature are summarized. The mechanisms that underlie the hyperthermic effects of MDMA in humans and treatment of severe hyperthermia are presented. The data show that MDMA produces an acute and dose-dependent rise in core body temperature in healthy subjects. The increase in body temperature is in the range of 0.2-0.8°C and does not result in hyperpyrexia (>40°C) in a controlled laboratory setting. However, moderately hyperthermic body temperatures >38.0°C occur frequently at higher doses, even in the absence of physical activity and at room temperature. MDMA primarily releases serotonin and norepinephrine. Mechanistic clinical studies indicate that the MDMA-induced elevations in body temperature in humans partially depend on the MDMA-induced release of norepinephrine and involve enhanced metabolic heat generation and cutaneous vasoconstriction, resulting in impaired heat dissipation. The mediating role of serotonin is unclear. The management of sympathomimetic toxicity and associated hyperthermia mainly includes sedation with benzodiazepines and intravenous fluid replacement. Severe hyperthermia should primarily be treated with additional cooling and mechanical ventilation.","PeriodicalId":22565,"journal":{"name":"Temperature: Multidisciplinary Biomedical Journal","volume":"47 1","pages":"192 - 200"},"PeriodicalIF":0.0,"publicationDate":"2014-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90265775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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